1.

01 Myocardial Infarction
DEFINITION: Death of the myocardium (cardiac muscle) resulting
from interruption of blood supply to that area of the myocardium

EPIDEMIOLOGY/RISK FACTORS
Epidemiology
Commonest cause of death in Australia
Indigenous rates higher
Risk factors
Previous MI (Most important factor)
Family history
Age
Male
Smoking
3 Hs = Hyperlipidemia , Hypercholesterolemia (LDL bad= low
is no!!) HTN (> 140/90)
Obesity / Sedentary lifestyle
Diabetes

AETIOLOGY
Disease of the intima: SMC migration from Media to Intima Intima
thickens and Media thins
Endothelial activation (HT, Smoking, Diabetes)
Platelet and Monocyte adhesion
LDL migrates through permeable endothelium (activated) and
become oxidated in the intima.
Vascular SMCs change phenotype from contractile to
proliferative/synthetic (platelet derived growth factor
response)
Macrophages and VSMC engulf lipids and become Foam cells
Atheroma
Necrotic core: No nuclei (dead cells)
Cholesterol clefts
Foam cells
Calcium presence (pathological calcification=
hardening of arteries)
Fibrous cap = VSMC and dense ECM (produced by VSMC)
Stable: thick cap
Unstable: thin cap (if vascular system highly
stimulated more likely to rupture)
Advanced Atherosclerosis
1. Rupture, ulceration, or erosion of cap (causes exposure of
collagen) thrombus or embolus formation
2. Aneurysm and rupture: Thinning media from VSMC
migration
3. Critical stenosis: Stable cap blocks the lumen and calcifies
PATHOGENESIS
Normal Myocardium Metabolism
Aerobic using Fatty acids (11% more O2 than glucose)
Creatine Phosphate (energy store)
Ischaemic Heart Conditions
No O2, fatty acids or glucose reaching cells
Fuel source from glycogen stores used anaerobically
(Glycolysis PYR LAC... NB. no krebs cycle)
LAC pH, PFK-1 (rate limiting enzyme in glycolysis)
Lack of fuel Ischaemic conditions in heart muscle
ATP active membrane pump failure Influx of Ca cell
death and lysis
Release of cell contents into blood stream
o
Trop I and T
o
CK (MB isoform; MM/BB isoforms more specific for
liver/brain disease)
o
LDH
Pain mediators: Bradykinins, Prostaglandins, Serotonin,
Histamine, LAC (pH) = sensitise or stimulate nociceptors which
travel with sympathetic fibres to spinal level T1-T4
Coagulative necrosis

Starts within 30 mins

Extensive within 2-6 hrs

CLINICAL FEATURES
History

Retrosternal chest pain (lasting > 30mins) (may come on at rest)

Referred pain to dermatomes T1-T4 (cardiac sensory

innervation sympathetic from T1-T4)

Dyspnoea

Palpitations

Syncope/ presyncope/ dizziness

Angor Animi (Anxiety), Nausea, Faintness, Restlessness.

Physical Exam:

Ankle swelling

Diaphoresis (sweating)

Hypotension accompanying Tachycardia (anterior infarction,

sympathetic hyperactivity) or Bradycardia (inferior infarction,
parasympathetic hyperactivity)

JVP (right ventricular infarction)

Dyskinetic apex beat (large anterior infarction).

intensity of heart sounds, murmurs, pericardial friction rubs

(transmural infarction)

DIAGNOSIS: Based largely on History; confirmed with investigations

Positive diagnosis requires two out of three findings in History,
ECG, Enzymes
Positive ECG findings are elevations of the ST segment and
changes in the T wave
Changes in Q wave show scarred heart tissue
Investigations
ECG
ST elevation
Pathological Q waves (previous infarction)
Serum markers
Troponin I and T from muscle = preferred marker
- Rises 3-12 hours, remains for 7-10 days
CK isoform MB
- Rises 4-8 hours, declines 12-24
LDH (converts pyruvate to lactate): L2 isoenzyme normally higher
that H4 >> flipped in AMI.
- Levels begin to rise 12-24 hrs and peak 2-3
FBC - General done
Chest X-ray
Cardiomegaly
Check for lung pathology or dissecting aneurysm
Echo/Angiogram
If needed for further investigation or diagnosis

TREATMENT/ MANAGEMENT
Short-term management

On arrival of suspected AMI: O2, Sublingual Glyceryl Trinitrate

(GTN) = Venous return + Vasodilate Cardiac Arteries, Aspirin
chewed, IV access blood sample for Markers and Biochem, 12
lead ECG

IV Morphine (opiate) for pain relief

Beta-blocker: for tachycardia

Glucose and insulin: fatty acid utilisation conserve O2

Angioplasty with stent: blows open blockage

Thrombolytic: streptokinase (if applicable)

Long-term management BANAS

B= Beta-blockers

A= Ace inhibitors

N= Nitroglycerides (Glycerol trinitrate)

A= Aspirin

S= Statins

Basic Sciences & Learning Topics

STRUCTURES OF THE CHEST
Pericardium - Two Layers:
[1] Tough outer fibrous layer - retains heart in position and limits
acute over distension of the chambers; attaches to the roots of the
great vessels above and behind, and to the diaphragm below
(therefore moves with inspiration/expiration).
[2] The Serous Pericardium - lies deep to the fibrous layer and
surrounds the pericardial cavity; Parietal layer lines the inner surface
of the fibrous layer and the visceral layer invests the heart

BOTH layers are continuous at the roots of the great

vessels. A thin film of fluid in the pericardial cavity
facilitates friction free movement of the heart.
Nerve supply
a) Parietal part of serous and the fibrous pericardium
Sensory innervation from Phrenic Nerve (C3-5).
b) Epicardium Autonomic Innervation from underlying heart

THE HEART INNERVATION

1. Sympathetic fibres from T1-4(5) regions of the spinal cord
HR & force of contraction.
2. Parasympathetic fibres from the vagus (CN X) HR
3. Efferent (motor) supply from autonomic nerves
4. Visceral afferents (sensory nerves from viscera) involved in
cardiac reflexes. Those subserving pain are stimulated by
ischaemia and accumulation of metabolic products. Travel with the
sympathetic nerves and enter the spinal cord at T1-4(5) levels Cardiac referred pain is therefore perceived as arising from the
skin supplied by those segments
Thoracic Wall
Inlet: T1, 1st rib and cartilage, manubrium
Outlet: T12, lower 6 ribs, xiphoid, diaphragm
Mediastinum
Superior contains great vessels, arch of aorta and 3 branches,
trachea (bifurcates at sternal angle), oesophagus, thoracic duct,
nerves (phrenic, vagus), thymus (adult)
Anterior ligaments, loose CT, Thymus (children)
Middle heart, pericardium, roots of great vessels, phrenic nerve
Posterior oesophagus (and vagal plexus), descending thoracic
aorta, thoracic duct
HYPOXIA, ISCHAEMIA AND CELL DEATH
Normal Conditions AEROBIC METABOLISM
Fatty acids, ketone bodies, lactate and pyruvate are oxidized CO2
+ H2O + ENERGY (transferred to ATP)
Creatine Phosphate is the energy store in cardiac and skeletal
muscle - made from ATP by creatine kinase (CK). The creatine
phosphate is used to maintain the level of cellular ATP to drive the
contractile process.
- At rest prefers Fatty Acids
- Under heavy workload, heart can also oxidise Glucose ATP
- Heart stores some glycogen that can be used under anaerobic
conditions
Ischaemia - insufficient blood supply of nutrients and O2 to muscle
decrease in supply and/or increase in demand
Levels of ATP can only be maintained to drive the contractile
process by breakdown of myocardial glycogen to glucose which then
is used to produce ATP via glycolysis.
PYR is normally completely oxidized to CO2 and H2O with
production of ATP
Ischaemic myocardium, it is converted to LAC (catalysed
by Lactate dehydrogenase) with a lower net yield of ATP
Pain and fatigue is attributed to glycolytically generated acid not
the lactic acid.
Ischaemia results in:
1. Intramuscular pH (7.0 6.4); [ATP] and [Cr Phos]
activity of PFK-1 (glycolytic enz) at this lower pH
2. To maintain function and viability, ATP is maintained by
myokinase (Adenylate Kinase; 2 ADP ATP + AMP).
Subsequent deamination of AMP by adenylate deaminase,
increases this production of ATP
If the oxygen absence continues: these temporary strategies also
become depleted and ATP dependent ion pumps in the outer
membrane of myoblasts cease to function, and the ion balance of the
cell is lost swell and burst release contents into the circulation
Next Few Weeks: Infarct is replaced by fibroblasts leaving a nonfunctioning fibrotic lesion

MECHANISMS OF PAIN
CARDIAC
Are sensory
releasedand
when
heart cells
are damaged
Pain isENZYMES:
an unpleasant
emotional
experience
associated with
actual or potential tissue damage, or an experience described in terms of
Troponin
and I - Contractile
proteins
of the myofibril.
The cardiac
such T
damage.
Pain is usually
associated
with the activation
of peripheral
isoforms
areby
very
specific for
injury
and or
are
notthe
present
in to do so,
nerves
a stimulus
thatcardiac
damages
tissue
has
potential
serum
from
people.
Troponins
preferedofmarkers
for
but
thehealthy
term "pain"
describes
bothare
thethe
perception
the nociceptive
event
detecting
myocardial
injury.
and the
personscell
psychological
response to it. Pain is highly subjective,
Troponin
(cTnI) orexperience
T (cTnT) are
the response
forms frequently
and aI persons
of and
to pain isassessed
strongly influenced
- previous
2 - 6 hours
after injury
by
experiences,
cultural and genetic background, gender and
Peaks instate.
12 - 16
hours
psychological
The
context in which the pain is experienced and the
cTnIofstays
elevated
for 5-10
cTnT for 5-14
intensity
the noxious
stimulus
aredays,
also important.
This days
can make
determining the severity of pain difficult, but untreated pain has significant
CK: Creatine
Kinase (creatine
phosphokinase)
- Enzyme
is foundstatus
in
adverse consequences
for the
physiological and
psychological
of
heartthe
muscle
(CK-MB
Isoform),
skeletal
muscle
(CK-MM),
andpain
brain an
patient,
particularly
if pain
becomes
chronic.
Chronic
(CK-BB).
CK and
in over
90%
of AMI.
However,
caneconomic
be in muscle
personal
social
burden
with
substantial
implications, and
trauma,
exertion,
postoperatively,
delirium
painphysical
specialists
consider
pain relief to convulsions,
be a basic human
right.
tremens
and other conditions.
Nociceptors:
Sensory nerves that detect noxious stimuli
Still Commonly
Assessed
Free
nerve endings, non adaptive (may lead to hyperalgesia)
stimuli:
in 4-6 hours post MI
Pain
- 1. Mechanical
peaks 24 hours
- 2. Thermal
Remains-elevated
foror
around
above 45c
below 3-4
12cdays
3. Chemical Direct stimulation:
CK - MB subforms
- This
is becoming
more
popular.
MB2 isEnzymes
BK,
5HT,test
HIST,
K+, H+, ACh,
ATP,
Proteolytic
Sensitisation:
Prostaglandins,
Substance
released from heart
muscle and converted
in blood
to MB1 P
[MB2]
= or >of
than
U/L indicates
MI up due to anaerobic
Ischaemia
as a cause
pain1.0
Lactic
acid build
MB2/MB1
ratio = orstimulation.
> than 1.5 indicates MI
metabolism
causes chemical
Nociceptive fibers in the heart project with the sympathetic nerves to the
Myoglobin
in striated
muscle.
Damage
skeletal
or cardiac
thoracic- Found
spinal cord
and also
via the
vagus to the
brainstem.
muscle
releases
into circulation.
There
are 2myoglobin
types of painJ
Time sequence after myocardial infarction
Rises fast (2 hours) after myocardial infarction
Peaks at 6 - 8 hours
Returns to normal in 20 - 36 hours
False positives Skeletal muscle injury and Renal Failure
LDH: Lactate Dehydrogenase
LDH peak at 3-4 days after MI
Remain elevated for up to 10 days
Useful for determining if a patient has had an MI if they present several
days after an episode of chest pain

DIFFERENTIAL DIAGNOSIS: CAUSES OF CHEST PAIN

PE, AMI, Cholecystits, Angina, GORD, Oesophageal Spasm
(Peacan Gos)
Angina due to low blood oxygen supply
- Dullness, heaviness and aching in a central retrosternal
location. Occurs on exertion (may occur at rest or during
sleep).
- Unaffected by respiration
- Relieved immediately by cessation of activity or within
minutes by sublingual nitrates
- Pain duration <30mins.
- ECG shows depression or elevation of the ST segment but
only when in pain. When not in pain, ECG is normal. Done
during exercise or for those who cant, a thallium scintigram is
used

MYOCARDIAL INFARCTION
more sever pain which comes on at rest
pain duration >30mins but does not last days.
assoc symptoms dyspnoea, diaphoresis (sweating),
angor animi (anziety), nausea, faintness, restlessness.
hypotension accompanying tachycardia (anterior infarction,
sympathetic hyperactivity) or bradycardia (inferior
infarction, parasympathetic hyperactivity).
Increased JVP (right ventricular infarction)
Dyskinetic apex beat (large anterior infarction).
decreased intensity of heart sounds, murmurs, pericardial
friction rubs (transmural infarction)
Positive diagnosis requires two out of three findings of history, ECG,
enzymes.
Positive ECG findings are elevations of the ST segment and changes
in the T wave. Changes in Q wave show scarred heart tissue.
Other Causes of Chest Pain
Gastro-esophageal reflux, oesophageal spasm, cholecystits.
Also pulmonary embolism

Mechanism of AMI
Contributing factors e.g. diet, smoking

Atherosclerosis
1) Endothelial insult (e.g. BP, radicals from
smoking)
activation of endothelium
secretion of adhesion molecules and
becomes leaky (cholesterol)
2) Fatty streak formed
3) Monocytes adhere to wall & migrate
intima become mature M
4) VSMCs phenotype & intima
5) VSMCs & M engulf lipid
foam cells
6) Eventually has necrotic core & fibrous cap
(thin cap = unstable)

Can rupture
tissue factor produced by

M & exposed collagen triggers platelet
adhesion & activation
thrombus

OCCLUSION OF CORONARY ARTERY

Myocardium deprived of O2
switched to
anaerobic metabolism:
+
Glu pyruvate lactate + H + little ATP
+
+
Pyruvate + NADH + H lactate + NAD
LDH catalyses this reaction. The isoforms of
LDH found in cardiac mm (H4, H3M etc) can thus
be measured

ATP production, lactate & acid production

OR
Vasospasm, emboli from LV
2+

CARDIAC MARKERS

Pain
Damaged tissue releases chemicals which
sensitise &/or stimulate nociceptors e.g.
bradykinin, PG, 5HT
nociceptors reach
threshold
AP dorsal horn (T1-4) BS &
higher centres
sensory & emotional
response

Ca pump fails
nuclear disruption,

mitochondrial swelling & dysfunction, activation of
proteolysis
plasma membrane blebbing =
coagulative necrosis.
* Cells start to die in ~ 30min, but have 2-6 hr
window til total cell death

Release of cell contents (including troponin, CK-MB)

SNS activity
sweating nausea etc

Criteria for the diagnosis of MI

1) Presenting Sx- pain is rapid onset, character (not sharp), location (central radiation), not relieved by GTN,
prolonged; associated dyspnoea, diaphoresis, nausea etc
2) ECG- May have ST elevation or depression, Q wave changes
3) Serum markers- Cardiac troponins (cTnT & cTnI) begin to rise 3-4 hrs after MI, peak 18-36 hrs, then slowly decline.
CK-MB rises at 3-8 hrs, peaks ~24hr, returns to normal within 48-72 hrs.
Need to take all this into account, but note that may be asymptomatic (silent MI) or may not have ECG change

Hypoxia, Ischaemia and Cell Death

GLYCOLYSIS

GG6PF6PF1,6BPDHAP+GAPJ 2 [ GAP1,3BPG3PG2PGPEPPYR ]

Glycolysis is a 10 stage processs catalyzed by a variety of enzymes and does NOT need O2 (occurs in the cytosol)

STEP
1
2
3
4
5
6
7
8
9
10

REACTION
G G6P
G6P F6P
F6P F1,6BP
F1,6BP DHAP + GAP
DHAP GAP
GAP 1,3BPG
1,3BPG 3PG
3PG 2PG
2PG PEP
PEP PYR

ENZYME
Hexokinase
Phosphoglucose isomerase
Phosphofructokinase (PFK) inhibited by pH
Alsolase
Triose phosphate isomerase
Glyceraldehyde 3-phosphate dehydrogense
Phosphoglycerate kinase
Phosphoglycerate mutase
Enolase
Pyruvate kinase

Up to stage 5, the process requires 2 ATP (adenosine 5'-triphosphate)

+
The process can be summarized as:
GLUCOSE + 2 ATP + 2 NAD 2 PYRUVATE + 4 ATP + 2 NADH
The final result is:
2 PYR 2 ATP 2 NADH
AEROBIC RESPIRATION (O2 present)
The NADH produced in glycolysis is used in the electron transport chain (ET; occurs in mitochondria).
+
ET uses electron donors (like NADH) to create a proton gradient that is used to make ATP and regenerates NAD for glycolysis.
ET is MUST have O2 to operate! It can make approximately 30 ATP from a single G!
ANAEROBIC RESPERATION (No O2 present)
+
Cells can make ATP using glycolysis because it doesnt need O2 but this is very inefficient and we still need to regenerate NAD . In
+
order to regenerate NAD , lactate dehydrogenase kicks in.
+
2 PYR + 2 NADH 2 LAC + 2 NAD
+
Although this process repays the investment of 2 NAD in glycolysis, it leaves us with a build up of lactate (lactic acid; a toxic dead end
by product that must enter gluconeogenesis in the liver)! pH then drops and PFK is inhibited!
ALTHOUGH HEART AND SKELETAL MUSCLE ARE BIOCHEMICALLY SIMILAR,
THE TWO TISSUES DIFFER METABOLICALLY.
Normal Conditions: metabolism in heart muscle (myocardium) is aerobic; fatty acids, ketone bodies, lactate and pyruvate are
oxidised to carbon dioxide and water with release of energy which is transferred to ATP. In cardiac and skeletal muscle, energy is
stored as creatine phosphate formed from the ATP by the enzyme creatine kinase (CK). The creatine phosphate is used to maintain the
level of cellular ATP to drive the contractile process of the myocardium, involving interaction of the proteins, actin and myosin. When
under a heavy workload, the heart can also oxidise glucose to form ATP but the resting heart preferentially oxidises fatty acids. The
heart stores some glucose in the form of glycogen which may be used under anaerobic conditions.
Myocardial ischaemia may occur when the blood supply of nutrients and oxygen becomes insufficient due either to a decrease in
supply or an increase in demand (or both). Blood flow to a portion of the heart may be interrupted by blockage of a coronary artery;
platelets from the blood may adhere to an atherosclerotic plaque resulting in formation of a thrombus which occludes the vessel. A
portion of the myocardium is deprived of nutrients and oxygen and levels of ATP to drive the contractile process can only be maintained
by breakdown of the myocardial glycogen to glucose units which can be used to produce small amounts of ATP via glycolysis.
Under aerobic conditions, the PYR is completely oxidised to CO2 and H2O with the production of ATP.
In ischaemic myocardium, the PYR is converted to LAC. However, the cardiac pain and fatigue associated with ischaemia is attributed
to glycolytically generated acid rather than lactic acid. The intramuscular pH may decrease from 7.0 to 6.4, levels of ATP and creatine
phosphate in cardiac muscle decrease due perhaps to a reduced activity of the glycolytic enzyme, PFK, at the lower cellular pH. To
maintain the function and viability of the myocardium a little longer, levels of ATP are maintained using the enzyme, myokinase
(adenylate kinase), which converts two molecules of ADP to ATP+AMP. Subsequent deamination of one of the products of the
myokinase reaction, AMP, by the enzyme, adenylate deaminase, increases this production of ATP.
However in the continuing absence of an oxygen supply, these temporary metabolic strategies also become depleted and ATPdependent ion pumps in the outer membranes of myoblasts cease to function, the ion balance of the cells is lost, they swell and burst,
releasing their contents into the circulation. Over the over next few weeks the infarct in the heart is replaced by fibroblasts leaving a
nonfunctional fibrotic lesion.
Two of the enzymes which appear in the blood stream after a myocardial infarction are lactate dehydrogenase (LDH) and creatine
kinase (CK), which exist as cardiac isozymes whose presence in the peripheral circulation confirms the occurrence of myocardial
infarction and may indicate its extent. Diagnostic tests have been developed to measure levels of LDH and CK in blood (serum
Toponins, however, are better markers of myocardial infarction).

1.01 Myocardial Infarction

SBAs: Myocardial Infarction

Case 8
You are waiting in a queue to pick up a ticket to the Rolling Stones
concert, when a man in his early 50s in front of you suddenly falls to
the ground unconscious. During your initial assessment you note that
his airway is clear, he is not breathing, he is pulseless and deeply
cyanosed.
33. The single most effective initial management step from the point
of view of cerebral oxygenation is:
A)
B)
C)
D)

Mouth-to-mouth assisted respiration

Chest compression
Loosening his top button
Placing him in the recovery position

Answer B
Curriculum Reference: 5.04 LT3
34. The most likely cause of the cyanosis in this case is:
A) Increased O2 uptake by the tissues
B) Cessation of respiration leading to inadequate O2 uptake
C) Absent circulation leading to O2 depletion in the tissues
D) Peripheral vasoconstriction due to air conditioning and cold
extremities
Answer C
A. Uptake of O2 by the tissues is presumably normal until O2 is
depleted
B. Whether or not respiration continued the subject would become
cyanosed in the absence of circulation
C. CORRECT
D. No particular relevance to the cyanosis in this case.
Curriculum Reference: 1.03 LT4
35. Which of the following findings will permit the earliest diagnosis of
myocardial infarction?

A) The presence of Q waves on ECG

B) ST segment elevation on ECG
C) Elevated serum troponin
D) Elevated serum creatine kinase
Answer B
A. Q waves take 12+ hours
B. ST elevation takes only minutes
C. Troponin takes usually 6-8 hours to rise
D. CK takes 3-4 hours to rise
Curriculum Reference: 5.04 LT3, Interactive ECG
36. The level of which one of the following biochemical species rises
with muscle ischaemia in the presence of circulatory failure?

A) ATP
B) Creatine phosphate
C) Glucose
D) Lactate
Answer D
In the context of ischemia, tissue oxygen availability falls, followed by
failure of oxidative phosphorylation. NADH is unused and its levels
build up driving conversion of pyruvate to lactate.

Curriculum Reference: 1.03.LT4

With appropriate interventions, he is resuscitated and rapidly

transferred to hospital by ambulance. The resident medical officer on
duty considers a diagnosis of acute myocardial infarction. An ECG is
performed on arrival in the Emergency Department. (results shown
opposite).
37. The ECG shows:

A) Acute anterior infarction

B) Left bundle branch block
C) Posterior infarction
D) Acute inferior infarction
Answer A
Curriculum Reference: 5.04 Interactive ECG
A diagnosis of acute myocardial infarction is made.
38. The most likely pathological basis for this mans myocardial
infarction is:

A) Coronary artery embolus

B) Thrombotic occlusion of a coronary artery
C) Dissection of a coronary artery
D) Coronary artery spasm
Answer B
Curriculum Reference: 5.04 LT3
Mr Jones wife Marian is contacted. When Marian arrives at the
hospital she is very anxious about her husband.

41. Assuming Mr Dickens has partial blockage of one of his coronary

arteries, which one of the following is an expected consequence?
A) Coronary arterioles downstream of the blockage
would be dilated by local metabolites
B) The pain is a consequence of intracellular lactic
acid stimulating pain receptors
C) Treatment with beta blockers would be beneficial
because they dilate coronary arteries
D) He can expect continued chest pain because
collateral vessels do not develop in the heart
Answer A
Reference: Regulation of blood flow to tissues 5.04 Lect 1
42. Mr Dickens artery wall is likely to contain each of the following
EXCEPT:
A) Immunologically active T-lymphocytes
B) Vascular smooth muscle cells that exhibit a
synthetic phenotype
C) A prominent infiltrate of neutrophils
D) Foamy macrophages
Answer C
Reference: 5.04, LT2 Genesis of atheroma
Blood tests reveal an elevated triglyceride level and low serum HDL.
43. Fibrates are a class of drugs that are of value in the treatment of
certain forms of hyperlipidemia. They reduce serum triglyceride levels
and elevate serum HDL cholesterol levels by binding to which one of
the following?
A) Cholesterol ester-transfer protein
B) Lecithin-cholesterol acyltransferase
C) Lipoprotein lipase
D) Peroxisome Proliferator-activated Receptor-alpha

39. Which one of the following effects is a consequence of anxiety?

A) Information processing is accelerated

B) Long term memory is improved
C) Sensory acuity is increased
D) Working memory is enhanced
Answer C
Sensory acuity is increased when people are anxious. The sense
organs become more sensitive to visual, auditory, olfactory, etc. stimuli
in order to prepare the individual to respond quickly to any
environmental threat posed by his/her surroundings. This aspect of the
anxiety response reflects the influence of evolutionary biology.
Curriculum reference: 1.03 LT 5 Communication in a medical
emergency
************************************************************************

Answer D
Fibrates bind to and activate PPAR-alpha with effects on both
triglyceride and cholesterol handling.
Curriculum Reference 5.04 Lecture 2.
**************************************************************************
Case 1
You have been visiting your accountant, Mr Welch, in his office.
Suddenly he falls to the ground unconscious. During your initial
assessment you note that his airway is clear, he is not breathing, he is
pulseless and deeply cyanosed.
1. The single most effective initial management step from the point of
view of cerebral oxygenation is:
A) Mouth-to-mouth assisted respiration
B) Chest compression
C) Loosening his top button
D) Placing him in the recovery position

Case 8
Michael Dickens is an 81 year old man who comes to you complaining
of 3 months of central chest pain, particularly when walking up a hill.
Investigations confirm your suspicion he has coronary artery disease.
40. Regarding coronary artery anatomy, which of the following is
correct?
A) The left coronary artery normally passes anterior to
the pulmonary trunk
B) The AV node of the heart is usually supplied by a
branch of the left anterior descending (anterior
interventricular) artery
C) The right coronary artery usually gives off the
posterior interventricular artery
D) The circumflex branch of the left coronary artery
supplies much of anterior wall of the heart
Answer C
Reference: 5.02 BCS1 Anatomy of the heart & great vessels

Answer B
Curriculum Reference: 5.04 LT3
2. The most likely cause of the cyanosis in this case is:
A) Increased O2 uptake by the tissues
B) Cessation of respiration leading to inadequate O2
uptake
C) Absent circulation leading to O2 depletion in the
tissues
D) Peripheral vasoconstriction due to air conditioning
and cold extremities
Answer C
A. Uptake of O2 by the tissues is presumably normal until O2 is
depleted
B. Whether or not respiration continued the subject would become
cyanosed in the absence of circulation
C. CORRECT
D. No particular relevance to the cyanosis in this case.
Curriculum Reference: 1.03 LT4

3. Which of the following findings will permit the earliest diagnosis of

myocardial infarction?
A) The presence of Q waves on ECG
B) ST segment elevation on ECG
C) Elevated serum troponin
D) Elevated serum creatine kinase

Answer A
Curriculum Reference: 5.04 Interactive ECG
A diagnosis of acute myocardial infarction is made.

Answer B
A. Q waves take 12+ hours
B. ST elevation takes only minutes
C. Troponin takes usually 6-8 hours to rise
D. CK takes 3-4 hours to rise
Curriculum Reference: 5.04 LT3, Interactive ECG
4. The level of which one of the following biochemical species rises
with muscle ischaemia in the presence of circulatory failure?
A) ATP
B) Creatine phosphate
C) Glucose
D) Lactate
Answer D
In the context of ischemia, tissue oxygen availability falls, followed by
failure of oxidative phosphorylation. NADH is unused and its levels
build up driving conversion of pyruvate to lactate.
Curriculum Reference: 1.03.LT4
ECG only in hard copy

With appropriate interventions, he is resuscitated and rapidly

transferred to hospital by ambulance. The resident medical officer on
duty considers a diagnosis of acute myocardial infarction. An ECG is
performed on arrival in the Emergency Department. (results shown
opposite).

5. The ECG shows:

A) Acute anterior infarction
B) Left bundle branch block
C) Posterior infarction
D) Acute inferior infarction

6. The most likely pathological basis for this mans myocardial

infarction is:
A) Coronary artery embolus
B) Thrombotic occlusion of a coronary artery
C) Dissection of a coronary artery
D) Coronary artery spasm
Answer B
Curriculum Reference: 5.04 LT3
Mr Welchs wife is contacted. When she arrives at the hospital she is
very anxious about her husband.
7. When patients and/or family members are anxious in a medical
consultation, communication can be impaired. Which one of the
following is characteristic of the effects of anxiety?
A) Information processing is accelerated
B) Working memory is improved
C) Sensory acuity is increased
D) Capacity to sustain attention is enhanced
Answer C
Sensory acuity is increased when people are anxious. The sense
organs become more sensitive to visual, auditory, olfactory, etc. stimuli
in order to prepare the individual to respond quickly to any
environmental threat posed by his/her surroundings. This aspect of the
anxiety response reflects the influence of evolutionary biology.
Curriculum reference: 1.03 LT 5 Communication in a medical
emergency
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